Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A human pancreatic beta cell tumor was maintained in monolayer cell culture for 80 days. The culture was terminated because of bacterial infection. Probably because extensive trypsin-collagenase dissociation was unnecessary, the dissociated cells attached much more quickly to the surface of the culture flask than do rat pancreatic cells obtained by enzymatic dissociation. Insulin release not only oscillated widely during the first 40 days of culture but also showed a decline from 380 mU the first week to about 50 mU/week the seventh week. For some unknown reason fibroblast overgrowth was not a major problem. Reduction of the medium glucose concentration from 16.5 mM to 5.5 mM did not alter insulin release rate. At glucose concentration of 16.5 mM, somatostatin 1.0 mug/ml reduced insulin release by 40%. From our previously reported studies on the effect of somatostatin on insulin release by monolayer cell cultures of rat endocrine pancreas, we conclude that the constant release of insulin by the tumor cells is relatively nonstimulated. We have confirmed that monolayer cultures of human pancreatic beta cell tumor do not represent a good model for normal human beta cell function because of the major shortcoming of an apparent inability to recognize glucose as a secretogogue.
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PMID:Monolayer cell culture of human pancreatic beta cell tumor: effect of glucose and somatostatin on insulin release. 17 3

The intraneutrophilic concentrations of lactoferrin, myeloperoxidase, collagenase and chymotrypsin-like cationic proteins were measured sequentially during acute bacterial infection. The serum levels of lactoferrin and myeloperoxidase were also followed as well as the 'eosinophil' cationic protein as a marker for eosinophil leucocytes. During the early course of infection there was a profound but reversible decrease of intraneutrophilic lactoferrin. The levels of cellular collagenase and chymotrypsin-like cationic proteins also tended to decrease reversibly during day 2-8 in most cases; myeloperoxidase levels were normal except for two cases. Serum myeloperoxidase and lactoferrin correlated with blood neutrophil counts. In spite of the absence of peripheral eosinophils the 'eosinophil' cationic proteins of serum were increased on the first day of infection, which may reflect increased eosinophil turnover.
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PMID:Neutrophil and eosinophil granulocytes in bacterial infection: sequential studies of cellular and serum levels of granule proteins. 20 75

The structural alterations elicited in the rabbit corneal stroma by experimental Serratia marcescens keratitis and by a highly purified serratia protease preparation were compared by gross observation, biochemical analyses, and electron microscopic examination of the affected tissue. Acute inflammation, liquefactive necrosis of the cornea, and descemetocele formation occurred during the development of the infection and after the intracorneal injection of submicrogram amounts of the protease. In vitro incubation of insoluble corneal stromal tissue with the bacterium or with the protease resulted in solubilization of the stromal proteoglycan ground substance; however, specific collagenase activity was not detected. Electron microscopic examination of corneas damaged by the bacterial infection and by the protease revealed loss of ruthenium red staining of the proteoglycan ground substance and dispersal of ultrastructurally normal collagen fibrils. Thus, our findings indicate that the major corneal damage which occurs during serratia keratitis and after the injection of the serratia protease is caused by solubilization and loss of the ground substance of the tissue. In addition, the observation that the major structural alterations observed during serratia keratitis can be reproduced by the bacterial protease supports the idea that the enzyme is involved, at least in part, with the production of severe corneal damage by the bacterium.
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PMID:Characterization of rabbit corneal damage produced by Serratia keratitis and by a serratia protease. 702 49

It is an important problem to associate bacterial infection in the process of bronchial stump healing. Wound healing processes in two types of bronchial stump closure methods, hand suturing with absorbable threads and mechanical stapling with stainless steel staples, were compared in mongrel dogs (154 dogs) which underwent right upper lobe reactions with and without infections. Half of the animals were infected with 10(9) CFU/dog of Pseudomonas aeruginosa E7 organisms. In order to understand the influence of bacterial infection on bronchial stump healing and also to evaluate the usefulness of the mechanical stapling device, we studied the number of viable bacteria, the activities of collagenase types I, II, III and IV, the amount of hydroxyproline and the histopathological finding in the bronchial stump tissue and the maximum leakage pressure. The number of viable bacteria decreased daily, but more than 10(3) CFU/g were detected even on the 21st day in infected dogs. There were no organisms detected in the stump tissues of uninfected dogs. The maximum leakage pressure levels by the 14th day after operation in the infected group were lower than in the uninfected group regardless of closure method. In the infected group of mechanical stapling the maximum leakage pressure increased daily, and on the 21st day became almost equal to that of uninfected group of mechanical stapling. The activity levels of collagenase type I in the infected group of both methods were at a maximum on the 5th day. On the same day the amount of hydroxyproline was at a minimum, and maintained a low level until the 14th day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of bacterial infection in bronchial stump healing and the usefulness of the mechanical stapling device]. 830 68

Vascular pathophysiology at the sites of bacterial infection and cancerous tissues share numerous common events similar to inflammatory tissue. Among them enhanced vascular permeability is the universal and hallmark event mediated by bradykinin. All 16 or more bacterial or fungal proteases we have examined activated one or more steps of the kinin generating Hageman-factor-kallikrein cascade. In the meantime, most of the microbial proteases rapidly inactivated various plasma inhibitors such as alpha 1-protease inhibitor and alpha 2-macroglobulin. In addition to the extracellular proteases, bacterial cell wall components (negatively charged LPS) of gram-negative bacteria and teichoic acid moieties of gram-positive bacteria activate the Hageman-factor-kallikrein system and exert hypotensive effects via kinin generation. Endotoxin (LPS) also induces nitric oxide synthase (NOS) which appears to exhibit a rather slow, but significant, effect in relaxing the vascular tone of the infected animal (thus hypotension). Furthermore, bacterial proteases can activate the matrix metalloproteinase (collagenase) resulting in exacerbation of tissue injury in the diseased animal. Many tumor cells or tissues excrete plasminogen activator, and hence activate plasminogen. The plasmin thus generated activates procollagenases, as well as the Hageman-factor-kallikrein system, resulting in pronounced extravasation. Fluid accumulation in pleural and ascitic carcinomatoses is largely due to the activated bradykinin-generating system. We can also demonstrate and control enhanced vascular permeability using kallikrein inhibitors, especially the polymer-conjugated soybean trypsin inhibitor which exhibits a prolonged plasma t1/2, kinin antagonists, NOS inhibitors, NO scavengers, inhibitors of prostaglandins and others. Bacterial proteases induce shock in mice which can be prevented by the soybean trypsin inhibitor by blocking the kallikrein-kinin cascade. Therapeutic use of kinin antagonists and a kallikrein inhibitor has been made for infectious diseases such as septicemia and in tumor pathology.
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PMID:Bradykinin and nitric oxide in infectious disease and cancer. 885 54

A reasonable interpretation of the present evidence indicates that diabetes, when a complication of periodontitis, acts as a modifying and aggravating factor in the severity of periodontal infection. Diabetics with periodontitis who were young and poorly controlled, those who were long-duration diabetics, especially those over 30 years old, demonstrated more attachment loss, bone loss, and deeper probing pocket depths than their nondiabetic controls. It seems that the earlier the onset of diabetes and the longer the duration, especially without consistent control, the more susceptible the individual will be to periodontal disease. Consequently, once a diabetic contracts periodontal disease, it is usually more destructive. Although plaque scores of diabetics may be comparable to or even less than those of nondiabetics, diabetics often exhibit higher gingival index scores. The elevation of this particular clinical parameter is indicative of the microangiopathy associated with diabetes. Diabetic microangiopathy contributes to compromised delivery of nutrients to surrounding tissues and poor elimination of metabolic waste products. The complications associated with diabetes such as macroangiopathy, microangiopathy (i.e., retinopathy), ketoacidosis, and hyperglycemia result in impaired wound healing, immunosuppression, and susceptibility to bacterial infection. Individuals ages 30 to 40 suffering from diabetic retinopathy had significantly more gingival inflammation than controls or diabetics without complications. Collagen metabolism is defective in diabetics and is one component underlying delayed wound healing. Animal studies have been instrumental in elucidating the details of delayed wound healing. Hyperglycemia was associated with increased collagenase and protease activity in the gingiva of rats. Vascular wound healing in rats, particularly new re-endothelialization across vascular anastomoses, was significantly impaired. Diabetic abnormalities in immune response include impaired neutrophil chemotaxis, phagocytosis, and adhesion. Decreased neutrophilic chemotactic response seems to be attributable to protein factors in diabetic serum that competitively bind neutrophil receptors, thereby preventing complement-mediated phagocytosis. Because diabetics are not able to eliminate circulating immune complexes (CIC) effectively, serum CIC levels are elevated. There are microbiological differences in the characteristic flora of NIDDM patients and IDDM patients with periodontitis. These differences are not associated with diabetic impaired immune response. Ultimately, bacterial plaque is the primary etiology of periodontal diseases. Evidently, the host's response to bacterial plaque and ability to heal following surgery is altered by diabetic disease. Therefore, a thorough history regarding onset of diabetes, duration, and diabetic control would prove useful in the clinical management of diabetics presenting for treatment of periodontal disease.
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PMID:Periodontal disease, diabetes, and immune response: a review of current concepts. 947 64

Interleukin-1 (IL-1) has been implicated as a participant in preterm labor that is induced by bacterial infection. Previously, we showed that serotonin-induced production of IL-1alpha by myometrial smooth muscle cells in vitro is also essential for the synthesis of interstitial collagenase. It is therefore likely that IL-1alpha production in uterine tissues has implications for both the normal physiology of involution and for the pathophysiological mechanisms of preterm labor. The objective of this study was to characterize the serotonin-induced production of IL-1alpha by myometrial cultures in vitro and to assess the production of IL-1alpha and its relationship to collagenase production in vivo during pregnancy and the postpartum period. Immunohistochemistry demonstrated IL-1alpha protein in the nuclei and cytoplasm of serotonin-treated myometrial cells. IL-1alpha levels were decreased by treatment with progesterone or IL-1-receptor antagonist but were unaffected by lipopolysaccharide. Western analysis of myometrium from pregnant rats showed low levels of IL-1alpha during midpregnancy with increased concentrations at days 21 and 22 and postpartum. IL-1alpha mRNA levels also increased from days 15 to 22. Levels of mRNA for IL-1beta also increased, although to a lesser degree than IL-1alpha. Both mRNAs decreased postpartum. Conversely, mRNA for interstitial collagenase was barely detectable at term but increased postpartum. Together, these data show that serotonin stimulates IL-1alpha production in vitro and indicate that normal myometrium from pregnant rats is an identifiable source of IL-1 during late pregnancy. The findings are consistent with the possibility that myometrial IL-1alpha participates in normal labor as well as the postpartum production of interstitial collagenase.
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PMID:Localization and regulation of IL-1alpha in rat myometrium during late pregnancy and the postpartum period. 1117 69

In vitro bioactivities of a beta-glucan produced by Panebacillus polymyxa JB115 were investigated. Nitric oxide production by RAW 264.7 macrophage cells pre-treated with beta-glucan JB115 (from 0.1 to 1 mg ml(-1)) was significantly increased, compared to that in untreated cells (P < 0.001). The beta-glucan JB115 increased superoxide radical-scavenging activity by 66% at 1 mg ml(-1). It also suppressed hyaluronidase (32%) and collagenase (33%) activities and, additionally, displayed antitumor activity, blocking the growth of Sarcoma 180 cells in a concentration-dependent manner. The immune-stimulatory, antioxidant, collagenase inhibitory and hyaluronidase inhibitory effects of the beta-glucan support its potential role in the prevention of bacterial disease against fish and in the protection of skin against aging.
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PMID:Physiological activities of a beta-glucan produced by Panebacillus polymyxa. 1842 27

PURPOSE. Trachoma, the leading infectious cause of blindness, is a chronic inflammatory scarring condition. Blindness follows the development of trichiasis, which is treated surgically. Unfortunately, it frequently recurs, compromising the treatment. In this study, gene expression analysis was used to examine factors that may be involved in the inflammation and tissue remodeling after surgery. METHODS. Subjects were examined before and at 1 and 4 years after surgery. Conjunctival swab samples were collected for bacterial culture, Chlamydia trachomatis PCR, and RNA isolation at 1 year. Quantitative real-time PCR was performed to measure the expression of tumor necrosis factor-alpha (TNF), interleukin-1beta (IL1B), matrix metalloproteinase-1 (MMP1), MMP-2, MMP-9, tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), TIMP-2, and hypoxanthine phosphoribosyl transferase-1 (HPRT1). RESULTS. Two hundred forty individuals with trachomatous trichiasis were recruited. One year after surgery, recurrent trichiasis was associated with a reduced MMP-1/TIMP-1 ratio (P = 0.029). IL1B expression was elevated in the presence of either conjunctival bacterial infection (P = 0.011) or inflammation (P = 0.002). TNF expression was greater in the Mandinka ethnic group (P < 0.0001), and it was increased when clinical inflammation was associated with nonchlamydial bacterial infection (P = 0.012). MMP-9 expression increased when conjunctival inflammation was associated with bacterial infection (P = 0.007). CONCLUSIONS. Recurrent trichiasis was associated with a reduced MMP-1 to TIMP-1 ratio, which may favor the accumulation of fibrotic tissue. Nonchlamydial bacterial infection may induce factors that contribute to conjunctival tissue remodeling and recurrent trichiasis in trachoma. Prospective studies are needed to assess the potential importance of these and other factors in progressive disease.
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PMID:Conjunctival expression of matrix metalloproteinase and proinflammatory cytokine genes after trichiasis surgery. 2023 45

Polyethylene glycol (PEG) has been previously shown to protect against enteric pathogens and prevent colon cancer invasion. To determine if PEG could indeed protect against previously observed pro-invasive effects of commensal E. coli and EPEC, Caco-2 cells grown in an in vitro model of colon cancer were infected with strains of human commensal E. coli or EPEC and treated with 10% PEG 3350, PEG 8000, and PEG 20,000, respectively. At 24 hours after infection, MMP-1 and MMP-13 activities, cell cluster thickness, depth of invasion, and proliferation were determined using standard molecular biology techniques and advanced imaging. We found that higher molecular weight PEG, especially PEG 8000 and 20,000, regardless of bacterial infection, increased proliferation and depth of invasion although a decrease in cellular density and MMP-1 activity was also noted. Maximum proliferation and depth of invasion of Caco-2 cells was observed in scaffolds treated with a combination of commensal E. coli strain, HS4 and PEG 8000. In conclusion, we found that PEG 8000 increased cell proliferation and led to the preservation of cell density in cells treated with commensal bacteria. This is important, because the preservation of a proliferative response in colon cancer results in a more chemo-responsive tumor.
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PMID:Higher molecular weight polyethylene glycol increases cell proliferation while improving barrier function in an in vitro colon cancer model. 2197 66


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